Papel do eosinófilo na patogênese da colite ulcerativa experimental em camundongos

• Ano de defesa: 2008
• Autor(a) principal: Angelica Thomaz Vieira
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Colite ulcerativa; Eosinófilo; Doenças inflamatórias intestinais; Resposta inflamatória; Imunologia; Bioquímica; Eosinófilos; Intestinos Doenças inflamatórias
• Link de acesso: http://hdl.handle.net/1843/BUBD-9GAFQL

Eosinophils are multifunctional pro-inflammatory leukocytes implicated in the pathogenesis of numerous inflammatory processes, including gastrointestinal disorders, but its precise role in the development of Ulcerative colitis is unknown. The present study was conducted to determine this role by using a mouse model of eosinophil lineage ablation (ÄdblGATA-1) and we choose oral administration of dextran sulfate sodium (DSS) to induce colitis. All WT mice died after DSS-induced colitis has been installed, while eosinophil deficient mice did not. Furthermore, eosinophil lineage ablation in mice has a protective effect in dextran sulfate sodium- induced colitis. Eosinophil accumulation was higher in WT mice with colitis than in ÄdblGATA-1 mice, as assessed by histopathological analysis and eosinophil peroxidase activity, even with high IL-5 levels in the latter group. Neutrophils accumulation was also significantly increased only in WT-treated with DSS. Furthermore, Eotaxin/CCL11, KC/CXCL1-3 and MIP-1á/CCL3 chemokines were increased in WT mice, compared to controls. However, theses chemokines showed no significant differences in ÄdblGATA-1 with colitis and controls. Thus, we suggest that eosinophils are critical in the development of gastrointestinal dysfunction, and mortality increase of mice submitted to experimental ulcerative colitis.